Non-alcoholic fatty liver disease (NAFLD) affects about a quarter of the world's population and it is closely linked to hypertension (HT). Pro-inflammatory and anti-inflammatory cytokines play a key role in the pathology progression, and the search for non-invasive biomarkers for the diagnosis of NAFLD remains an important issue.
The aim of the study was to determine the diagnostic and prognostic value of IL-1β and IL-10 in assessing the progression of liver parenchyma changes in patients with NAFLD and HT comorbidity.
Materials and methods. A study of 115 patients with non-alcoholic steatohepatitis (NASH) was performed. The main group consisted of 63 patients with NASH and HT, 52 patients with isolated NAFLD represented the comparison group. Clinical and laboratory parameters were evaluated, IL-10 and IL-1β levels were measured by ELISA method, ultrasound steatometry and elastography were performed in all patients.
Results. The attenuation coefficient and median liver stiffness in NAFLD and HT group significantly exceeded the results in the isolated NAFLD group and in the control group. The IL-1β level in NAFLD and HT group was 17.55 pg/ml, and in isolated NAFLD group the indicator averaged 15.72 pg/ml, which exceeded the control values (8.26 pg/ml). IL-10 level was 12.69 pg/ml and 14.34 pg/ml in patients with comorbid and isolated NAFLD, respectively, while control results averaged 16.19 pg/ml. It were found strong relationship between IL-1β, IL-10 and CRP levels in patients with NAFLD and HT (r=0.61, p=0.024, and r=-0.69, p=0.036, respectively). Inverse correlations were also found between the cytokines IL-1β and IL-10 in NAFLD patients with and without HT (r=-0.61, p<0.001, and r=-0.57, p<0.001, respectively). Changes in the cytokine status of patients with NAFLD at different stages of steatosis and liver fibrosis had been identified.
Conclusions. The presence of concomitant HT in patients with NAFLD is associated with greater severity of liver parenchyma changes. NAFLD manifestation is accompanied by increase of IL-1β and decrease of IL-10 levels, and deepening of these deviations were found in patients with comorbidity of NAFLD and HT.
Interleukins IL-1β and IL-10 can be defined as biomarkers of NAFLD progression both in its isolated course and in its comorbidity with HT. The possibility of using biomarkers as an independent non-invasive test of diagnosing NAFLD requires further study.
Background and AimNon-alcoholic fatty liver disease (NAFLD) is closely linked to hypertension (HT). An important issue remains the search for non-invasive tests to NAFLD detection in the early stages of liver fibrosis. The objective of the study was to evaluate the diagnostic and prognostic value of kallistatin in assessing the liver fibrosis progression in NAFLD and HT patients.Patients and Methods115 patients with NAFLD with and without HT were examined, the control group consisted of 20 relatively healthy volunteers. Plasma kallistatin level measurement, ultrasound steatometry and elastography were performed in all patients.ResultsKallistatin level was 65.03 ng/ml (95% CI 61.38; 68.68), 83.42 ng/ml (95% CI 81.89; 84.94) and 111.70 ng/ml (95% CI 106.14; 113.22) in patients with NAFLD and HT, isolated NAFLD and control group, respectively. There were significant differences in the liver parenchyma condition between groups. Kallistatin levels strongly inversely correlated with the attenuation coefficient and the mean liver stiffness in NAFLD and HT (rs=-0.70) and in the isolated NAFLD patients (rs=-0.56; rs=-0.68, respectively). Kallistatin level was 71.82 ng/ml (95% CI 70.16; 79.51) and 58.62 ng/ml (95% CI 55.81; 64.45) in patients with HT stage I and HT stage II, respectively (p<0.001).ConclusionsConcomitant HT in NAFLD patients is associated with greater severity of fatty and fibrotic liver changes. The course of NAFLD is accompanied by decrease in kallistatin level. Increased degree of liver steatosis and fibrosis, inflammation activity, increased BMI and increased stage of HT lead to inhibition of kallistatin activity. Kallistatin may be considered as a biomarker for progression assessment of NAFLD with or without HT.
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